REVIEW OF HEMATOLOGY.pdf

SHALOM UNIVERSITY INC
NAME: YINKFU MARCEL NDAMNSAH AND DR SHEI CLAUDE NFOR
TEL: 676945988
EMAIL: YINKFUMARCEL02@GMAIL.COM
FIELD OF STUDY: MEDICAL LABORATORY SCIENCE
OPTION: BACHELOR OF SCIENCE IN M.L.S.
SCHOOL: SHALOM UNIVERSITY

UNIT ONE
HEMATOCRIT
Definition: Hematocrit is also known as packed cell volume is the volume of red
blood cell in blood. It is just a percentage of your red blood cell.
When blood is centrifuge in a 1mm tube, it is separated into three compartments
i.e. red blood, cell, buffy coat, and plasma represented diagrammatically below;
-Red blood cell layer: Also called erythrocytes and there are about 5.6 million
RBCS per microliter of blood. The normal hematocrit which is 45% is gotten by
dividing 0.45ml/1ml x 100 where 0.45ml is the quantity of RBCs present in a 1mm
hematocrit tube. When the hematocrit level of an individual is measured and is
above 45%, it is termed polycythemia and when it is below normal it is called
Anemia.
-Buffy coat layer: consist of two types of formed elements platelets and white
blood cell which accounts for 1% of total fraction of whole column.

Platelets also called thrombocytes play an important role in blood clotting. In an
apparently healthy individual there are about 150000-450000 platelets per micro
liter of blood. A platelet count of greater than 450000 per microliter of blood is
termed thrombocytosis and a count of less than 150000 is termed
thrombocytopenia.
White blood cell also called leucocytes has a normal range of 4800-11000 cells per
microliter of blood. When the white blood cell count is greater than 11000, it is
termed leukocytosis and when it is below 4800 cells per microliter is termed
leucopenia.
-Plasma layer: it is the liquid part of blood and accounts for about 55% of total
blood components. This percentage is gotten by 0.55ml/1ml x 100 where 0.55ml is
the quantity of plasma present in a 1mm hematocrit tube after centrifugation.
Plasma is mainly water(93%), plasma protein(7%) mainly albumin which regulate
water levels of blood, globulins( alpha and beta globulins) which are transport
proteins, also present are gamma globulins which are produce by plasma B cells.
Inside plasma is also oxygen (O2), carbon dioxide (CO2), nitrogen monoxide,
electrolytes (calcium, potassium, sodium, chloride, etc.), nutrients (example
glucose, fatty acid, proteins, and amino acids), enzymes, hormones, and metabolic
waste product such as lactic acid.

UNIT TWO
ERYTHROPOEISIS
Definition: it is the normal production of red blood cells and it occurs in the
epiphysis of the red bone marrow. Red blood cell production is driven when there
is;
-Blood loss
-Less availability of oxygen at the level of the tissues (hypoxia)
-Anemia and other causes
For erythropoiesis to occur, iron is the most specific component. Other components
include; proteins, enzymes, B12, folic acid (B9) and the hormone erythropoietin.
Iron is the main component of hemoglobin and in blood Fe2+
is converted to Fe3+ by
Dewamo cytochrome B and the product formed id later reduced to Fe2+ .
A divalent
metal transport protein binds IBO ferritin with iron and converts it to ferritin and
iron is released in the bone marrow, ferritin in turn is later to hemosiderin is

released out of bone marrow as a Ferro-protein molecule which is needed for the
transport of oxygen. Papasten converts Fe2+
to Fe3+
which binds to hepcedein
which is a transport protein transports the iron to the spleen, bone marrow, liver.
Present in the duodenum is B12 and folic acid. The parietal cells of the stomach
makes protein called the intrinsic factor which binds to B12 in the stomach and is
released into the blood stream. Amino acids, fats, also called transcobalamin
produce at the level of the digestive tract is absorbed along the duodenum and in
the blood stream we have amino acids, carbohydrates, fats, B12, and folic acid.
At the level of the Bowman’s capsule of the kidney, transcription factor called the
hypoxia inducible factor binds to EPO (erythropoietin gene) and cause the release
of EPO by the kidneys into blood.
At the bone marrow where blood cells are produced is what is called stem cells or
hemocytoblast or pluriportent stem cell. EPO produced by the kidneys move to the
bone marrow and trigger myeloid tissue to produce red blood cells. EPO is
genetically programmed to produce genetic red cells. The diagram below
schematically represents the production of erythrocyte when the myeloid tissue is
triggered by EPO.
Red blood cell transports respiratory gases i.e. oxygen from the lungs to the tissues
and carbon dioxide from the tissues to the lungs. After production, erythrocyte
lives for 100-120 days. B12 and folic acid are essential for DNA maturation in the
process of RBC formation and when there is lack of these nutrients megaloblastic
anemia will set in. Amino acids is essrntial for DNA synthesis while fats are
essential for hemoglobin synthesis

UNIT THREE
LIFE SPAN OF ERYTHROCYTE AND DESTRUCTION
Life span of Erythrocyte
Red blood cell has a lifespan of about 100-120days. After 120 they are destroyed
and new ones are formed.
Red blood cell Destruction
After 120 days, certain proteins called spectrin (red protein) and ankrin (yellow
protein) allows for change in structure and deformation of erythrocyte. At the level
of the spleen, macrophages which are phagocytes engulf old red blood cell, digest
them and breaks them into haem and into two alpha and two beta globin chains.
RBCs are also destroyed by the Kuppfer’s cells of the liver. The globin chains
consist of amino acids and these amino acids are later recycled for another cycle of
erythrocyte production.
The haem contains iron and eboferritin. Ferritin combines with other ferritin
molecules to form a cluster of ferritin molecules called hemosiderin. Bliverdin
from haem part is converted to bilirubin which is toxic and cannot be transported
in blood so it binds to plasma protein albumin (bilirubin + albumin) and the
complex formed now is called indirect bilirubin or unconjugated bilirubin. The
unconjugated bilirubin is then conjugated in the liver by glucoronic acid. The
bilirubin formed is called direct or conjugated bilirubin which is non-toxic to
human calls. The gall bladder produces bile which mixes with conjugated bilirubin
and at the level of the small intestines, bacteria release an enzymes proteases
which breaks down bilirubin into urobilinogen and it is reabsorbed back into the
blood stream and is ecreted by the kidneys as urobilin. Some of the urobilinogen is
broken down in the intestines into stercobilinogen and is excreted as stercobilin in
stool. When urobilinogen is present in the intestines, it is called
fecostercobilinogen. If bilirubin is pushed into blood stream, jaundice results.

UNIT FOUR
TYPES OF ANEMIA
What we shall be looking into are listed below
-review of anemia
-iron deficiency anemia (microcytic)
-pernicious anemia (B12/folic acid) macrocytic anemia
-Hereditary spherocytosis
-G6PDH
-sickle cell anemia
-hemorrhagic anemia
-aplastic (pancytopenia)
-Thalassemia (microcytic) anemia
Anemia
Definition of anemia
Anemia is a term used to describe when there is low oxygen carrying capacity. It
also refers to decrease red blood cell mass. This happens due to decrease number
of red blood cells, low packed cell volume or low hematocrit.
The types of anemia are described below:
A) Iron Deficiency Anemia
Iron deficiency anemia is defined as a decrease in the amount of red blood cells or
hemoglobin due to not enough iron.
Signs and Symptoms of Iron Deficiency Anemia
-Dyspnea (shortness of breath)

- increase workload in the heart causing tachycardia
- Dizziness
The component protopoferrin 9 reacts with Fe2+
to form heam. So when iron
content is deficient less haem will be produced leading to the production of
microcytic red blood cells. In iron deficiency anemia the mean corpuscular volume
is less than 80femto liter. The mean corpuscular volume is gotten by
MCV= hematocrit x 10 and the product divided by total red blood cells.
If an individual MCV is below 80fl, then the person is suffering from microcytic
anemia or microcytosis.
Causes
-blood loss, ulcer
-heavy menstrual bleeding
-not enough iron in your diet.
Treatment
-blood transfusion
C) Pernicious Anemia (B12/Folic acid), Macrocytic Anemia

One way pernicious anemia can develop is by loss of gastric parietal cells, which
are responsible for the secretion of the intrinsic factor, a protein that is essential for
the absorption of B12 in the small intestine. If antibodies at the level of the
stomach bind to the intrinsic factor, they block the action of B12 and B12 is
needed for DNA maturation in the process of erythropoiesis, as a result leading to
the production of RBCs with larger size (Macrocytic RBCs). Macrocytic RBCs are
RBCs with larger size than normal. Since the action of B12 is blocked and it’s not
bound to an intrinsic factor, there will be deficiency of B12. In this type of anemia,
the mean corpuscular volume is greater than 100fl.
Treatment
-Intramuscular injection of B12.
D) Hereditary Spherocytosis
This is a disorder caused by mutations in genes relating to membrane proteins that
allow for the erythrocyte to change shape. Spectrin and other membrane proteins
plays an essential rule in maintaining the normal shape of red blood cell and when
deficient causes mutation in the shape of RBCs and it takes a spherical shape.

Signs and Symptoms
-Splenomegaly
E) G6PDH (Glucose-6-phosphate Dehydrogenase) Deficiency
G6PDH is an enzyme produce by the liver that helps red blood cells to work
properly and deficiency of the enzyme causes hemolytic anemia (destruction of red
blood cells). This enzyme plays an important role in energy supply to the cells of
the body by maintaining the level of NADPH. Deficiency of G6PDH leads to a
defect in NADPH production. When NADPH levels are low, it will lead to low
levels of GSH that result in oxidative damage to blood cells leading to hemolysis.
In this type of anemia there is production of Heinz bodies which causes decrease
flexibility of RBCs.
Below is the schematic representation of G6PDH, NADPH formation;
Laboratory Tests
-Combs test

E) Sickle cell Anemia (HbS).
Sickle cell disease and its variance are genetic disorders resulting from the
presence of mis-sense mutation of hemoglobin gene, HbS. Normal hemoglobin
(HbA) has two alphas and two beta globin chains link together. Sickle cell RBCs
results when normal hemoglobin molecules polymerize to sickle shape due to
missense mutation.
Patients with sickle cell disease often go into vaso-occlusive crisis which occurs
when sickle red blood cells block blood flow to the point that tissues become
deprived of oxygen and patients present with mild to severe pain with variable
intensity.
Treatment of Patients suffering from sickle cell anemia
-give oxygen
-pain relievers
-intravenous fluids can be administered
-hydroxyl urea can be given

F) Hemorrhagic Anemia
Hemorrhagic anemia occurs when there is decrease in red blood cell due to blood
loss resulting from gastrointestinal bleeding caused by helicobacter pylori, or as a
result of gunshot wounds, etc.
Treatment
-blood transfusion
-treating PUD patients
G) Aplastic Anemia (Pancytopenia)
At the level of the bone marrow are myeloid and lymphoid cells. The myeloid
precursors produce red blood cells, white blood cells abundantly neutrophil and
thrombocytes while the lymphoid tissue produces lymphocytes.
Aplastic anemia occurs when the hemocytoblast of the bone marrow cannot make
enough red blood cells and white blood cells leading to a drop in hemoglobin.
Causes
-Epstein Barr virus
-Drugs
Pancytopenia is a generalized term for low white blood cells, low red blood cells
and low platelets.
An individual with aplastic anemia has an increased risk of bruising, infection, etc.
Treatment
-blood transfusion
-bone marrow transplant
G) Thalassemia (microcytic)

It is a genetic condition common with the mediterenians. The normal hemoglobin
is HbA which has two alpha and two beta globin chains. Thalassemia sets in when
the alpha or the beta chain is missing in the hemoglobin molecule. Alpha (α)
Thalassemia is a disorder that occurs when there is absence of one (1) alpha globin
chain i.e. 1α and 2β globin chains present in the hemoglobin molecule. Beta (β)
occurs when 1β is absent in a hemoglobin molecule i.e. 2α and 1β.
With Thalassemia, MCV is less than 90femtolitres leading to microcytic anemia.
Treatment
-iron supplement
-stem cell transplant
-blood cell transfusion

UNIT 5
POLYCYTHERMIAS
This is a condition that occurs when there is increases production of red blood
cells.
When the stem cells of the bone marrow are destroyed or are cancerous, they tend
to produce more red blood cells than normal leading to increase hemoglobin level
in blood. Since there are more red blood cells present in the vascular capillaries,
there is a greater risk of thromboembolism, risk of developing high blood pressure,
etc. Since the blood is highly viscous, some of it can become emboli and find it
way to the lungs causing pulmonary embolism.
Signs and symptoms of polycythemia
-increase viscosity of blood
-increase blood pressure
-increase bleeding
-increase incidence of thrombi or emboli
-having longer prothrombin time
There are two main types of polycythemia i.e. primary polycythemia and
secondary polycythemia
A) Primary polycythemia
This type occurs when there is a problem in the stem cells of the bone marrow, it
could be due to mutation that produce red blood cells leading to over production of
red blood cells. The most common type is polycythemia vera. This condition leads
to high production of hemoglobin as a result of increased erythropoiesis and also
due to a dysfunction or hyper function of the JAK-STAT pathway leading to more
erythrocyte.
B) Secondary polycythemia: This type of polycythemia develops as a response to
chronic hypoxia which triggers increased production of EPO by the kidneys

leading to increase red blood cell production. When there is a cancer within the
kidneys, cardiovascular diseases will trigger increase EPO and increase JAK-
STAT pathway.

UNIT SIX
LEUCOPOEISIS
Leucopoiesis is the process of forming white blood cells from the pluripotent,
hematopoietic stem cells of the bone marrow. This process id stimulated by various
colony stimulating factors which are hormones produced by mature white cells.
Leucopoiesis is divided into two categories of stem cells namely myeloid stem cell
and the lymphoid stem cell.
-Myeloid stem cell. This stem cell differentiates leading to the formation of white
blood cells monocytes, neutrophils, basophils, and eosinophil’s. The myeloid stem
cell also produces megakaryoblast essential for the formation of platelets
(thrombocytes) which is not a type of white blood cell but is essential for the
normal functioning of the body.
-Lymphoid stem cell: This cell differentiates producing lymphocytes.
There exist five types of white blood cells namely neutrophils, eosinophil’s,
monocytes, basophils, and lymphocytes. They perform specific functions some of
which are;
-Transport of nutrient, respiratory gases, etc.
-Fight against diseases by producing antibodies. Some are macrophages which
phagocytize bacteria and parsites present in the body.
Regulation of body temperature within normal limits.
How the process of leucocytes formation is represented schematically below;

Monocytes
-very good antigen presenting cells
-alveolar macrophages

- has a bean-shape structure
-Normal value: 3-8%
Basophils
-produces heparin which is an anticoagulant
-Release histamine, which regulates information and inflammation.
-highly granulated and at times the granules obscure the cytoplasm
-Normal value: 0.5-1%
Eosinophils
-secret protein which kills parasites and worms
-Type one hyper-sensitivity mediator
-Two lobes arranged in a spectacular manner
-its granules are thicker than that of neutrophils and appear orange.
-Normal value: 2-4%
Neutrophils

-Great phagocytes
-Take oxygen and convert to super oxide and then hydroxide radical.
-Have about 2-4 lobes and its granules are pink in color.
-Normal value: 50-70%
Platelets (thrombocytes)
-blood clotting preventing blood loss
-Normal value; 150000-450000cells/microliter
Lymphocytes
-B-lymphocytes secret antibodies that fight diseases
-T-lymphocytes help B-lymphocytes to produce antibodies and the cytotoxic T-
cells that destroy antigenic cells.
-Normal value: 20-30%

UNIT SEVEN
HEMOSTASIS
Definition: Hemostasis is the stoppage of blood flow from a ruptured blood vessel.
When there is a rupture of blood vessels, the endothelial cells secret chemicals
called nitric oxide PGI2 and their purpose is to inhibit platelets from binding into
the endothelial lining. Glycoseminolycin, heparin sulphate binds to another protein
anti-thrombin iii degrading clotting factor ii, ix, meanwhile factor iii, x, and ix are
activated. Thrombomycin binds to thrombin and initiates the process of
hemostasis.
Mechanism of hemostasis
(i)Vascular spasm
(ii) Platelet plug formation
(iii) Coagulation
(iv)Clot retraction and
(v) Fibrinolysis
When tissues are damaged;
1: Vascular spasm: When tissues are damage the endothelia mechanism is initiated
which causes the release of certain chemicals that binds to the endothelial cells and
brings about contraction. This happens in two ways;
-Myogenic mechanism: contraction of smooth muscles.
-Norciceptor activation: to activate the body’s response to blood loss
The Von Willebrand factor binds to glycoprotein-B1 is glycoprotein present in
blood and cause the release of adenosine diphosphate (ADP), thromboxane-A2,
serotonin. ADP, thromboxane-A2, have receptors on their membrane that binds to
platelets and bring about platelet aggregation. Thromboxane-A2 and serotonin
binds and cause muscle contraction leading to vasoconstriction hence vascular
spasm.

2: Platelet plug formation
The presence of phosphate group on endotherlial cell membrane brings about
platelet plug.
Platelet plug formation occurs in two pathways;
A) Intrinsic pathway: This pathway takes about 4-6 minutes and begins when
factor xii interact with negative charges on platelets and activates factor xi, factor
xi activates factor ix, factor ix activates factor xiii. Factor x reacts with factor v to
form a complex which activates prothrombin. The activated prothrombin reacts
with prothrombin factor to give factor ii (thrombin).
Thrombin converts soluble fibrinogen to insoluble fibrin which slows flow of red
blood cells. Factor xiii in the presence of calcium (Ca2+
) causes cross linking of
fibrin leading to a fibrin mesh.
B) Extrinsic pathway: This pathway last only for 30 seconds
-Tissue factor IV activates factor iii
-factor iii secreted by damaged tissue cells activates factor vii
-factor vii reacts with factor iii to yield factor ix and they become activated.
3. Coagulation/ (4) clot retraction and repair
- Platelet contraction
-secretion of a chemical called platelet derived growth factor which triggers
regeneration of collagen fibers and proliferates the smooth muscle.
- Secretion of vascular endothelial growth factor, which regenerates new
endothelial lining.
5. Fibrinolysis: it is the normal breakdown of fibrin clot

In this phase, tissue plasminogen activator reacts with plasminogen and leads to
plasmin and this complex degrade fibrin mesh and release an important peptide
called D-dimer.

UNIT SEVEN
BLOOD TYPING
Certain antigens present on the surface of individual red blood cells are responsible
for blood typing. These antigens are antigens A, B and the Rh. An individual’s
blood type is determined after an agglutination (clumping of red blood cells) test
using blood group antisera. The various blood types and how they can be
determined are explained below;
1) Blood group A
- Has antigen-A on red blood cell surface
- has antibodies B in its plasma
a) A Rhesus positive (A+
)
Can donate to;
A+
, AB+
Can receive from;
A+
, O-
, A-
, O+

b) A Rhesus negative (A-
)
Can donate to;
A-
, AB-
, AB+
Can receive from;
A-
, O-
2) Blood group B
-has antigen-B on the surface of its red cells
-Has antibody-A in plasma
a) B Rhesus positive (B+
)
Can donate to;
-B+
, AB+
Can receive from;
B+
, O+
, B-
, O-
b) B Rhesus negative (B-)
Can donate to;
B-, AB+, AB-
Can receive from;
B-
, O-
3. Blood group AB
- Has antigens A and B on its red cell surface
- Has no antibody against antigens A, B in plasma
The presence or absence of Rh antigen makes an individual AB Rh- or AB Rh+

A) AB Rhesus negative (AB-
)
-Can donate to;
AB-
, AB+
-Can receive from;
A-
, B-
, AB-
, O-
b) AB Rhesus positive (AB+
)
-Can donate to;
AB+
-Can receive from;
A+
,A-
,B+
,B-
,AB+
, AB-
, O+
, O-
4. Blood group O
- Has no antigen on the surface of their red cells
- Has antibodies A and B in plasma
a) O Rhesus negative (O-
)
-Can donate to;
A+
, A-
, B+
, B-, AB+
, AB-
, O+
, O-
-Can receive from;
O-
b) O Rhesus positive (O+
)
-Can donate to;
A+
, B+
, AB+
, O+
-Can receive from;

O+
, O-
Hemolytic Disease of the new born (erythroblastosis foetalis)
-This condition comes about when a woman who is Rhesus negative is pregnant
for a Rhesus positive baby.
- No problem in the first birth but serious problem in subsequent births.
- During delivery of the first child, maternal blood mixes with fetal blood and the
Rhesus positive (Rh+) leaks into the mother’s circulation.
- The mother’s immune system produces anti-rhesus antibodies (memory
antibodies, IgG) for any subsequent rhesus positive pregnancy.
-The antibody IgG cross the placenta and attacks the baby’s red blood cells leading
hemolytic anemia.
Treatment

-Anti-rhesus antibody called RHOGAM can be administered within 48 hours after
delivery of the first child. RHOGAM binds to the anti-rhesus antibody, IgG
produced in the mothers system and prevent damage to the fetal red blood cells.

UNIT NINE
APPROACH TO ANEMIA
Life cycle of Red blood cells
There are certain hormones that drive erythrocyte production;
-The hormones T3 (thyroxin) and T4 (tryiodothyronine)
-Erythropoietin to drives RBSs production
-Folic acid, iron, and B12 essential for the production of RBCs
Toxins if present in the bone marrow inhibit the activity of the bone marrow to
produce RBCs or even damage the red bone marrow. This activity will cause the
stem cells to produce low RBCs as result leading to anemia. Since there is blood
loss, the toxins if present in stem cells of the bone marrow will trigger more red
blood cells to balance what is being lost causing intravascular and extravascular
hemolysis.
Normal bone marrow, there is red blood cell production in normal numbers and
blood flows to the entire system and if someone has a blood loss as result of
gastrointestinal bleeding or any other means, the red blood cells will be low
because you are losing them. This cause the RBCs to be low, low hematocrit
leading to anemia. Since blood is lost, the stem cells of the red bone marrow will
produce more RBCs. This type of anemia is often called anemia due to decrease
hormones, B12, folic acid, iron. This will cause the reticulocyte index to increase,
i.e. greater 2%.
When your bone marrow is not working properly, all the other blood types will not
be properly formed. This could lead to anemia as a result of cancer of the bone
marrow or bone marrow damage. In this type the reticulocyte (immature RBCs)
will be less than 2%
Anemia due to decrease production

This occurs as a result of decrease production of the hormones erythropoietin, T3
and T4, B12, folic acid, iron. In this type of anemia, there is low RBCs, low
hematocrit, and decrese nutrients.
-Reticulocyte index is ordered as a test and if it is less than 2%, there is a
reticulocyte problem and if the reticulocyte index is greater than 2%, it indicates
increase bone marrow activity due to blood loss or destruction problem.
-MCV= hematocrit x 10 divided by total RBCs and normal MCV is 80-100fl. If an
individual’s MCV is less than 80fl, it is termed microcytic anemia and if the MCV
is between 80-100fl (normocytic anemia) and if greater than 100fl it is termed
macrocytic anemia.
Tests
-RDW,
-Mean cell index
-Iron studies
-Peripheral blood smear
Iron deficiency anemia
-RDW is high and RBCs is low
-Mean cell index is greater than 30
MCI=MCV/total RBCs
-Iron studies (ferritin usually low, transferrin saturation is high)
Microcytic Anemia
Iron deficiency anemia, thalassemia and anemia of chronic disease will cause red
blood cells to be smaller than normal a condition called microcytic anemia.
Tests
-RDW

-RBC count
-Mean cell index
-Iron studies
-Peripheral blood smear
Anemia of chronic disease
This is a type of anemia that occurs as a result of the kidney malfunction leading to
decrease production of EPO.
Tests
-RDW: low
-RBCs: low
-Ferritin levels: high
Thalassemia
A disorder of hemoglobin that arise as a result of the absence of one alpha or one
beta globin chains that make up a hemoglobin molecule.
Tests
-RDW: high
-RBC is normal
-Mean Cell Index: less than 30%
Sickle Cell Anemia
-PBS: sickle cells
-Hb-electrophoresis: HbS
Membrane Problem

-PBS: spherocytes
-Medical history
Micro-angiopathic Hemolytic Anemia
It a process of red blood cell destruction within the microvasculature brought about
by thrombocytopenia (low platelets count i.e. below 150000) due to platelet
activation and consumption causing HEEPs syndrome, mechanical valve problem
and DIC (Disseminated intravascular coagulopathy)
Tests
-Platelet count: low
-TTP; low
-LFPs: high
-PBS: schistocytes
Signs and Symptoms of low platelets
-High fever
-Myalgia
-As a tick bite, the PBS of this patient shows ghost cells due to cell death.
Case study
1)75 Y/O M presents with mechanical thrombectomy for stroke has Hgb of 6.8g/dl
-RI: 7%,
-LDH: normal
-Haptoglobin: normal
-Indirect bilirubin; normal
Diagnosis; microangiopathic hemolytic anemia

2)75 Y/O M with PMH of CLL presents with Hgb of 8.9g/dl.
-RI; 9%
-LDH: high
-Haptoglobin; normal
-Indirect bilirubin; high
-DAT: positive for TgG (immunoglobulin G)
Diagnosis; warm AIHA (autoimmune hemolytic anemia) likely 2/2 cell
3) 75 Y/O M with cough, SOB, green sputum production with an Hgb of 9.9g/dl.
-RI: 6%
-Haptoglobin: low
-Indirect bilirubin: high
-DAT: negative for TgG and positive for compliments and IgM
Diagnosis: Cold AIHA, PCR (polymerase chain reaction) can be ordered for
confirmation.

UNIT TEN
APPROACH TO POLYCYTHEMIA
Polycythemia arises when there is increased hemoglobin, hematocrit, and increased
red blood cells due to over production of hormones responsible for red blood cell
production and also as a result of high production of EPO by the kidneys that leads
to over production of red blood cells, hyperactivity of the bone marrow producing
more red blood cells than normal.
Stimulants
-Kidney problem or liver problem
-Low oxygen in tissues
-Lung problem
-Less oxygen in the atmosphere
-Heart issue
In certain disorders of the heart that is pulling deoxygenated blood into the system,
P50 test can be done to check the hemoglobin oxygen carrying capacity to rollout
hemoglobinopathy.
Tests to check for Polycythemia
-Red blood cell mass whether it is normal (relative erythrocyte) and if high then
primary polycythemia.
-If EPO is high then its secondary polycythemia. If EPO is low, then its primary
polycythemia whereby there is inhibition of EPO as a result of over production of
hormones responsible for RBC formation.
-JAK-STAT mutation and if positive, then it is primary polycythemia.
In high altitudes, there is limited amount of oxygen i.e. Low oxygen carrying
capacity in the body since it is smaller amount in the atmosphere. For this
individual, check medical history, oxygen saturation, also do CT scan of the liver,

abdomen, head, etc. The CT scan is done to check for renal cell carcinoma or
hepatocellular.

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